Higher intakes of the B vitamins thiamine and riboflavin from the diet may reduce the incidence of premenstrual syndrome (PMS) by about 35 percent, suggest new findings. According to a new paper published in the American Journal of Clinical Nutrition, the link between B vitamins and PMS is biologically plausible since B vitamins such as thiamine and riboflavin are known to play important roles in the synthesis of various neurotransmitters involved in PMS.

While most women experience mild emotional or physical premenstrual symptoms, as many as 8-20 per cent of women experience symptoms severe enough to meet the definition of premenstrual syndrome, which can substantially interfere with daily activities and relationships. The new study, performed by researchers from the University of Massachusetts, Harvard, and the University of Iowa, indicates that increase intakes of certain B vitamins from food sources may help reduce the incidence of PMS.

Using data from 1,057 women with PMS and 1,968 women without PMS participating in the Nurses' Health Study II cohort, the researchers found that women with the highest average intakes of riboflavin two to four years prior to diagnosis were associated with a 35 percent lower incidence of PMS than women with the lowest average intakes. On the other hand, the researchers did not observe any benefits with other B vitamins, including niacin, folate, B6, and B12. In addition, supplemental intakes of these vitamins was not linked to PMS incidence, they added. “We observed a significantly lower risk of PMS in women with high intakes of thiamine and riboflavin from food sources only,” wrote the researchers. “Further research is needed to evaluate the effects of B vitamins in the development of premenstrual syndrome.”

Beyond the B vitamins, there is also some evidence for the potential of a diet rich in calcium and vitamin D to lower the risk of developing PMS, a condition that affects up to a fifth of all women. According to a study published in 2005 in the Archives of Internal Medicine (Vol. 165, pp1246-1252), researchers from the University of Massachusetts and GlaxoSmithKline reported for the first time that calcium and vitamin D may help prevent the initial development of PMS.

Scientists may have discovered a way of identifying dieters who are prone to piling the pounds back on after weight loss. A study at Maastricht University’s Department of Human Biology found a link between a gene involved in regulating blood pressure and post-diet weight gain in women. Women who regained weight after slimming had a high change in the concentration of a particular protein in their blood during dieting, research showed. Researchers now hope to develop a test to indicate how prone people are to yo-yo dieting.

Edwin Mariman, professor of functional genetics at Maastricht, said: “It was a surprising discovery, because until now there has been no clear link between this protein and obesity. “We do not yet have an explanation for the results, but it does appear that it should be possible within a few years to use this finding to develop a test to show who is at high risk of putting weight back on after a diet.”

Hospitals already conduct tests for the protein, known as the angiotensin I converting enzyme (ACE). But the test is currently carried out to check its activity in regulating blood pressure, rather than its concentration. Up 80% of dieters suffer from the yo-yo effect, returning to their original weight within a year.

The study looked at around 100 women aged 20 to 45, half of whom had maintained their post-diet weight and half of whom had put weight back on. The findings of the research have been published by Dr Ping Wang, a scientist in Professor Mariman’s research group, in the online scientific journal PloS ONE.

Eating a diet rich in fibre has long been known to help keep your digestive tract working properly. It’s also thought to lower the risk of heart disease, some cancers and diabetes. Now, a new study suggests it could reduce the risk of death from cardiovascular, infectious and respiratory diseases. People who ate a high-fibre diet decreased their risk of dying over a nine year period compared to those who ate less fibre, according to a new study in the Archives of Internal Medicine.

The findings are based on a diet study from the National Institutes of Health and AARP, which included 219,123 men and 168,999 women ages 50 to 71 when the study began. Researchers from the National Cancer Institute examined food surveys completed by the participants in 1995 or 1996. After nine years about 11,000 people died and researchers used national records to determine the cause.

People who ate at least 26 grams per day were 22 percent less likely to die than those who consumed the least amount of fibre — about 13 grams per day or less. Men and women who consumed diets higher in fibre also had a reduced risk of cardiovascular, infectious and respiratory diseases, the study found. Getting fibre from grains seemed to have the biggest impact, the authors write.

The study has some limitations — mainly, people who ate high-fibre diets might also have been more likely to eat healthier diets overall, attributing to their longevity. Still, the study offers more evidence that fibre is certainly good for you. Federal dietary guidelines recommend people consume at least 14 grams of fibre per 1,000 calories, so about 28 grams for an average 2,000 calorie-per-day diet. But many experts say many people don’t get enough.

Addiction researchers at Washington University School of Medicine in St. Louis have found that a risk for alcoholism also may put individuals at risk for obesity. The researchers noted that the association between a family history of alcoholism and obesity risk has become more pronounced in recent years. Both men and women with such a family history were more likely to be obese in 2002 than members of that same high-risk group had been in 1992. “In addiction research, we often look at what we call cross-heritability, which addresses the question of whether the predisposition to one condition also might contribute to other conditions,” says first author Richard A. Grucza, PhD. “For example, alcoholism and drug abuse are cross-heritable. This new study demonstrates a cross-heritability between alcoholism and obesity, but it also says — and this is very important — that some of the risks must be a function of the environment. The environment is what changed between the 1990s and the 2000s. It wasn’t people’s genes.”

Obesity in the United States has doubled in recent decades from 15 percent of the population in the late 1970s to 33 percent in 2004. Obese people – those with a body mass index (BMI) of 30 or more – have an elevated risk for high blood pressure, diabetes, heart disease, stroke and certain cancers.

Reporting in the Archives of General Psychiatry, Grucza and his team say individuals with a family history of alcoholism, particularly women, have an elevated obesity risk. In addition, that risk seems to be growing. He speculates that may result from changes in the food we eat and the availability of more foods that interact with the same brain areas as addictive drugs. “Much of what we eat nowadays contains more calories than the food we ate in the 1970s and 1980s, but it also contains the sorts of calories — particularly a combination of sugar, salt and fat — that appeal to what are commonly called the reward centers in the brain,” says Grucza, an assistant professor of psychiatry. “Alcohol and drugs affect those same parts of the brain, and our thinking was that because the same brain structures are being stimulated, overconsumption of those foods might be greater in people with a predisposition to addiction.”

Grucza hypothesized that as Americans consumed more high-calorie, hyper-palatable foods, those with a genetic risk for addiction would face an elevated risk from because of the effects of those foods on the reward centers in the brain. His team analyzed data from two large alcoholism surveys from the last two decades. The National Longitudinal Alcohol Epidemiologic Survey was conducted in 1991 and 1992. The National Epidemiologic Survey on Alcohol and Related Conditions was conducted in 2001 and 2002. Almost 80,000 people took part in the two surveys.

“We looked particularly at family history of alcoholism as a marker of risk,” Grucza explains. “And we found that in 2001 and 2002, women with that history were 49 percent more likely to be obese than those without a family history of alcoholism. We also noticed a relationship in men, but it was not as striking in men as in women.” Grucza says a possible explanation for obesity in those with a family history of alcoholism is that some individuals may substitute one addiction for another. After seeing a close relative deal with alcohol problems, a person may shy away from drinking, but high-calorie, hyper-palatable foods also can stimulate the reward centers in their brains and give them effects similar to what they might experience from alcohol.

“Ironically, people with alcoholism tend not to be obese,” Grucza says. “They tend to be malnourished, or at least under-nourished because many replace their food intake with alcohol. One might think that the excess calories associated with alcohol consumption could, in theory, contribute to obesity, but that’s not what we saw in these individuals.” Grucza says other variables, from smoking, to alcohol intake, to demographic factors like age and education levels don’t seem to explain the association between alcoholism risk and obesity. “It really does appear to be a change in the environment,” he says. “I would speculate, although I can’t really prove this, that a change in the food environment brought this association about. There is a whole slew of literature out there suggesting these hyper-palatable foods appeal to people with addictive tendencies, and I would guess that’s what we’re seeing in our study.” The results, he says, suggest there should be more cross-talk between alcohol and addiction researchers and those who study obesity. He says there may be some people for whom treating one of those disorders also might aid the other.

It's no secret that eating well is good for both body and mind, so it may not come as a surprise that a new study finds women who eat more olive oil and leafy vegetables such as salads and cooked spinach are significantly less likely to develop heart disease.A group of Italian researchers found that women who ate at least 1 serving of leafy vegetables per day were more than 40 percent less likely to develop heart disease over an average of eight years, relative to women who ate two or fewer portions of those vegetables each week. Women who downed at least 3 tablespoons of olive oil daily – such as in salad dressing – were also 40 percent less likely to be diagnosed with heart disease, compared to women who ate the least olive oil.

It's not exactly clear why specifically leafy vegetables and olive oil may protect the heart, said study author Dr. Domenico Palli of the Cancer Research and Prevention Institute in Florence. “Probably the mechanisms responsible for the protective effect of plant-origin foods on cardiovascular diseases involve micronutrients such as folate, antioxidant vitamins and potassium, all present in green leafy vegetables.” Folate reduces blood levels of homocysteine, Palli explained, which is thought to increase the risk of cardiovascular disease by damaging the inner lining of arteries. Other studies have shown people who eat more potassium have lower blood pressure, which can protect the cardiovascular system. Virgin olive oil may be particularly effective at lowering heart disease risk because of its high level of antioxidant plant compounds, he added.

This is not the first study to link olive oil or vegetables to good heart health. Most famously, the traditional Mediterranean diet — rich in vegetables and monounsaturated fats from olive oil and nuts, but low in saturated fat from meat and dairy — has been tied to a decreased risk of heart disease. Mediterranean-style eating has also been credited with lowering risk for some cancers, diabetes, and, more recently, with slowing brain aging. Cardiovascular disease is a major killer, responsible for 30 percent of all deaths worldwide and the leading cause of death for both men and women in the U.S.

To look more closely at the role of foods in protecting against heart disease, Palli and colleagues reviewed dietary information collected from nearly 30,000 Italian women participating in a large national health study. Researchers followed the women, whose mean age was 50 at the beginning of the study, for an average of 8 years, noting who developed heart disease. In that time, the women experienced 144 major heart disease-related events, such as heart attack or bypass surgery, the authors report in the American Journal of Clinical Nutrition. Women who ate at least one daily serving (about two ounces) of leafy vegetables – such as raw lettuce or endives, or cooked vegetables like spinach or chard — had a 46 percent lower risk of developing heart disease than women who ate at most two portions per week. Consuming at least an ounce of olive oil per day lowered their risk by 44 percent relative to women who consumed a half-ounce or less daily, the authors found.

The women's intake of other types of vegetables, such as roots and cabbages, and their consumption of tomatoes or fruit did not seem to be linked to their risk for major heart events. Both fruits and vegetables have been associated with heart benefits in past studies conducted elsewhere in Europe and in North America. The authors caution that the apparent lack of positive effect from high fruit consumption in their results may have something to do with a different attitude toward fruit in Italy. It is cheap, varied and easily available, so eating a lot of fruit is a widespread habit but it does not necessarily signal that the rest of someone's diet is as healthy, the authors wrote. Another issue with the study, Palli noted, is that women had to report how much they ate of various items, and some may not have remembered their diets accurately, or may have changed their eating habits during the study period. In addition, people sometimes over-estimate their healthy behaviors, believing they eat healthier than they really do.

SOURCE: American Journal of Clinical Nutrition, published online December 22, 2010.

Alzheimer’s disease, a major form of dementia, has no cure. Luckily, diet and lifestyle can be modified to reduce the risk. For instance, Mediterranean diet and physical activity may each independently reduce the risk of the condition, according to a study in the Aug 2009 issue of Journal of American Medical Association. Dr. N. Scarmeas and colleagues of Taub Institute for Research in Alzheimer’s Disease and the Aging Brain and Department of Neurology at Columbia University Medical Center found men and women those who adhered most closely to Mediterranean diet were 40 percent less likely to be diagnosed with Alzheimer’s disease during a average of 5.4-year follow-up, compared to those who adhered to the diet least closely.

The researchers also found those who most actively engaged in physical activity were up to 33 percent less likely to be diagnosed with Alzheimer’s compared with those who were least active. For the study, Scarneas et al. followed 1880 community-dwelling elderly people who lived without dementia at baseline in New York for their dietary habits and physical activity.

Adherence to a Mediterranean-style diet was assessed on a scale of 0-9, or trichotomized into low, middle, or high and dichotomized into low and high. Physical activity was trichotomized into no physical activity, some, and much and dichotomized into low and high. Neurological and neuropsychological measures were conducted about every 1.5 years from 1992 to 2006. During the 5.4-year follow-up, 282 incident cases of Alzheimer’s were identified.

Those who adhered to the Mediterranean diet with a high score were at 40 percent reduced risk of Alzheimer, compared to those on the diet with a low score. A Mediterranean diet with a middle score did not seem to help compared to a diet with a low score. Those who engaged in some physical activity or much physical activity were at a 25 percent or 33 percent reduced risk of Alzheimer’s disease, respectively, compared with those who did no physical activity. Men and women who had neither followed Mediterranean diet nor much physical activity had an absolute Alzheimer’s risk of 19 percent. This is compared to 12 percent for those who followed both high scored Mediterranean diet and engaged in much physical activity – a difference of 45 percent.

Women consuming too much red meat may have a higher risk of stroke than women eating less, says a new study. Red meat is high in saturated fat and cholesterol; both are risk factors for cardiovascular disease, heart attack, and stroke. The United States Centers for Disease Control and Prevention suggests lowering saturated fat intake and eating more fresh fruits and vegetables to help reduce your risk of stroke. Writing in the journal Stroke, researchers examined nearly 35,000 Swedish women, ages 39 to 73. None of the women had heart disease prior to the start of the study in 1997.

After ten years, results showed 4% of the study participants, 1,680 women, had a stroke. Those consuming the most red meat had the highest risk of stroke. Women in the top tenth of red meat intake, consuming at least 3.6 ounces each day, were 42% more likely to have a stroke, compared to women who ate just under one ounce of red meat daily.

Eating processed meat also increased stroke risk. Women eating 1.5 ounces of processed meat each day were 24% more likely to suffer a cerebral infarction, compared to woman consuming less than half an ounce of processed meat each day. Processed meat was not linked to any other form of stroke. Cerebral infarction is a type of stroke caused by a disturbance in the blood vessels supplying blood to the brain. Other types of stroke involve a rupturing of a blood vessel, called hemorrhagic strokes.

The scientists blame red meat and processed meat’s effect on raising blood pressure for the increased stroke risk. According to the World Health Organization (WHO), every year an estimated 17 million people die due to cardiovascular diseases, most notably stroke and heart attack. The WHO lists physical inactivity and unhealthy diet as the main risk factors for heart disease and major cardiac events.

New research may help explain why multiple sclerosis rates have risen sharply in the U.S. and some other countries among women, while rates appear stable in men.The study could also broaden understanding of how environmental influences alter genes to cause a wide range of diseases. The causes of multiple sclerosis (MS) are not well understood, but experts have long suspected that environmental factors trigger the disease in people who are genetically susceptible. In the newly published study, researchers found that women with MS were more likely than men with MS to have a specific genetic mutation that has been linked to the disease.

Women were also more likely to pass the mutation to their daughters than their sons and more likely to share the MS-susceptibility gene with more distant female family members. If genes alone were involved, mothers would pass the MS-related gene to their sons as often as their daughters, said researcher George C. Ebers, MD, of the University of Oxford. Ebers’ research suggests that the ability of environmental factors to alter gene expression — a relatively new field of genetic study known as epigenetics — plays a key role in multiple sclerosis and that this role is gender-specific.

The theory is that environmental influences such as diet, smoking, stress, and even exposure to sunlight can change gene expression and this altered gene expression is passed on for a generation or two. “The idea that the environment would change genes was once thought to be ridiculous,” Ebers says. “Now it is looking like this is a much bigger influence on disease than we ever imagined.”

The study by Ebers and colleagues included 1,055 families with more than one person with MS. Close to 7,100 genes were tested, including around 2,100 from patients with the disease. The researchers were looking for MS-specific alterations in the major histocompatibility complex (MHC) gene region. They found that women with MS were 1.4 times more likely than men with the disease to carry the gene variant linked to disease risk. A total of 919 women and 302 men had the variant in the MHC region, compared to 626 women and 280 men who did not have it.

The study appeared in the Jan. 18 issue of Neurology.

Epigenetics is not evolution. Genetic alterations linked to environmental assaults can be passed down for a generation or two, but DNA usually rights itself over time, Ebers says. “This may explain why we hardly ever see MS in families over more than three generations,” he says. Earlier studies by Ebers and colleagues suggest that vitamin D deficiency may be the environmental stressor that triggers the MS-linked gene alterations. Rates of the disease are highest among people living farthest from the equator, and there is widespread speculation that lack of vitamin D due to low sun exposure may explain this. Other than Ebers’ research team, Orhun Kantarci, MD, of the Mayo Clinic in Rochester, Minn., is one of the few researches studying epigenetics as it relates to multiple sclerosis.

Kantarci calls the new research a potentially important piece of the puzzle to explain the gender difference in MS, but he adds that the research must be replicated. “This study provides more questions than answers, but it is very interesting,” he says. “We are learning that inheritance isn’t as simple as [Gregor] Mendel described.”

A popular pastime for many older people is to try and figure out their chances of getting one ailment or another. Mayo Clinic researchers have simplified it – they have figured out the lifetime risk of developing rheumatoid arthritis and six other autoimmune rheumatic diseases for both men and women. “We estimated the lifetime risk for rheumatic disease for both sexes, something that had not been done before — separately or collectively,” says Cynthia Crowson Mayo Clinic biostatistician and first author. “Prevalence and incidence rates existed, but prevalence figures underestimate individual risk and incidence rates express only a yearly estimate.”

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The researchers were looking for an accurate basis to offer an easy-to-understand average risk over a person’s lifetime, knowing that risk changes at almost every age. They used data from the Rochester Epidemiology Project, a long-term epidemiology resource based on patients in Olmsted County, Minn. The cohort of 1179, consisted of patients diagnosed between 1955 and 2007, allowed the team to extrapolate the nationwide estimates.

The adult lifetime risk in the United States of having some kind of inflammatory autoimmune disease is 8.4 percent for women and 5.1 percent for men. Based on year 2000 population figures, that means one woman in 12 and one man in 20 will develop one of the conditions in their lifetime. The authors consider that a substantial risk and say their findings should encourage more research on the value of early diagnosis and intervention for people with increased genetic risk of arthritis. They hope the new figures will help in counseling patients and in fundraising efforts to find improved treatments.

The most common type of breast cancer in older women — estrogen and progesterone receptor (ER/PR) positive breast cancer — has been linked to a protein that fends off aging-related cellular damage. A new study led by Vanderbilt-Ingram Cancer Center researcher David Gius, M.D., Ph.D., now shows how a deficiency in this aging-associated protein may set the stage for these tumors to develop.

The findings, published in Molecular Cell, provide information that could assist in the screening, prevention and treatment of these common age-related cancers. While the young are certainly not spared cancer’s wrath, cancer is primarily a disease of aging, with the majority of cases occurring in people over 50. However, the biological processes that underlie this association are not clear.

“The connection between aging and cancer is one of the most established phenomena in cancer research,” said Gius, associate professor of Cancer Biology, Pediatrics and Radiation Oncology. “The problem to address this clinically significant question is that this field lacks in vivo models to study this.”

In the late-1990s, proteins called “sirtuins” were linked to extended lifespan observed in several species maintained on a calorically restricted diet. These nutrient-sensing sirtuin proteins seemed to defend against aging-related cellular damage. Sirtuins are present in all living organisms, with humans having seven different sirtuin proteins. “When (the sirtuins) were discovered, it seemed obvious to conclude that there might be a mechanistic connection between the genes that determine length of survival and cancer,” Gius said. Previously, while at the National Cancer Institute, Gius and colleagues created mice lacking some of these sirtuins.

They reported last January in Cancer Cell that when they knocked out Sirt3 — a sirtuin localized in the mitochondria, the cellular “power plants” — the mice developed ER/PR positive breast tumors, the most common type of breast cancer in postmenopausal women. These tumors also exhibited increased levels of damaging free radicals and “reactive oxygen species” (ROS) — including superoxide, the primary metabolite of oxygen in the mitochondria — which provided an important clue as to how Sirt3 deficiency might permit these tumors to develop. “The mechanism, at least in part, for why these mice develop receptor positive breast cancer is altered mitochondrial ROS, including superoxide,” Gius said. But how deficiency in a longevity gene led to increased ROS was not clear. Since superoxide is generally removed from the cell with the help of a detoxifying enzyme called manganese superoxide dismutase (MnSOD), Gius hypothesized that the Sirt3 deficiency may abnormally regulate MnSOD.

In the current study, the researchers show that Sirt3 knockout mice have decreased MnSOD activity despite having normal levels of the protein. Gius and colleagues determined that the MnSOD in Sirt3 knockout mice was abnormally modified (with a chemical “acetyl” group) at a specific amino acid (lysine 122). This aberrant modification of MnSOD reduced the enzyme’s ability to detoxify superoxide and appeared to explain the increase in ROS in Sirt3 knockout mouse tumors. “These results suggest that aberrant regulation of MnSOD plays a role in receptor positive breast cancer,” said Gius.

Gius and colleagues also developed an antibody that can assess the acetylation status of MnSOD, which he says can potentially be used “to screen breast tissue samples to determine what women are at risk for (receptor positive) cancer or for recurrence because of this dysregulation of MnSOD.” Additionally, agents that target the acetylation of this amino acid on MnSOD may be useful as chemopreventive therapies in women at risk of these cancers and of recurrence, he noted. The research was supported by grants from the National Cancer Institute and the Department of Defense.